Human cytomegalovirus infection inhibits response of chronic hepatitis-C-virus-infected patients to interferon-based therapy
Noha G Bader El Din
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorMai Abd El Meguid
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorAshraf A Tabll
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorMohamed A Anany
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorGamal Esmat
Department of Tropical Medicine, Faculty of Medicine Cairo University, Cairo, Egypt,
Search for more papers by this authorNaglaa Zayed
Department of Tropical Medicine, Faculty of Medicine Cairo University, Cairo, Egypt,
Search for more papers by this authorAmr Helmy
Department of Surgery, National Liver Institute, Menoufia University, Menoufia, Egypt
Search for more papers by this authorAbdel Rahman El Zayady
Department of Internal Medicine, Faculty of Medicine, Ain Shams University, Cairo, Egypt,
Search for more papers by this authorAhmed Barakat
Department of Microbiology, Faculty of Science, Ain Shams University, Cairo, Egypt, and
Search for more papers by this authorCorresponding Author
Mostafa K El Awady
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Dr Mostafa El-Awady, Department of Biomedical Technology, National Research Center, El-Behooth Street 12622, Dokki, Giza, Egypt. Email: [email protected]Search for more papers by this authorNoha G Bader El Din
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorMai Abd El Meguid
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorAshraf A Tabll
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorMohamed A Anany
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Search for more papers by this authorGamal Esmat
Department of Tropical Medicine, Faculty of Medicine Cairo University, Cairo, Egypt,
Search for more papers by this authorNaglaa Zayed
Department of Tropical Medicine, Faculty of Medicine Cairo University, Cairo, Egypt,
Search for more papers by this authorAmr Helmy
Department of Surgery, National Liver Institute, Menoufia University, Menoufia, Egypt
Search for more papers by this authorAbdel Rahman El Zayady
Department of Internal Medicine, Faculty of Medicine, Ain Shams University, Cairo, Egypt,
Search for more papers by this authorAhmed Barakat
Department of Microbiology, Faculty of Science, Ain Shams University, Cairo, Egypt, and
Search for more papers by this authorCorresponding Author
Mostafa K El Awady
Department of Biomedical Technology, National Research Center, Cairo, Egypt,
Dr Mostafa El-Awady, Department of Biomedical Technology, National Research Center, El-Behooth Street 12622, Dokki, Giza, Egypt. Email: [email protected]Search for more papers by this authorAbstract
Background and Aim: Cytomegalovirus (CMV) is a ubiquitous pathogen that infects the majority of humans. Co-infection of CMV and hepatitis C virus (HCV) may deteriorate the prognosis of HCV-infected patients. This study was conducted to examine the role of CMV reactivation in determining the response rate to treatment with interferon and ribavirin therapy in chronic HCV patients.
Methods: Viral loads and genotyping were assessed using reverse transcription polymerase chain reaction and Innolipa systems, respectively. Reactivation of CMV in HCV patients who were all positive for CMV immunoglobulin G antibodies was tested by amplification of the gB1 gene using the end-point dilution quantitative-nested polymerase chain reaction method.
Results: CMV DNA was detected in 89.7% of non-responders and in 34.6% of sustained virological responders. Patients with reactivated CMV had significantly higher fibrosis scores (72.7%) than those with undetectable CMV DNA (23.8%, P = 0.002). Patients with positive CMV had higher rates of non-response and relapse (79.5%) than those with negative CMV DNA (19%). Chronic HCV patients with latent CMV had higher rates of response (81%) to treatment than those with reactivated CMV (20.5%, P < 0.001). Therefore, HCV patients with reactivated CMV and advanced fibrosis were least likely to achieve a sustained virological response following interferon therapy. This possibility is reduced to 50% of its original value in patients with reactivated CMV without fibrosis.
Conclusions: Besides the staging of liver fibrosis, CMV co-infection should be considered as an extremely important factor when designing predictive models for HCV response to interferon treatment.
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